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Biomedical subjects

E Bürgisser

Publications and source records attributed to E Bürgisser.

At least 19 recordsLinked to original sources
PubMed1992

[Oat bran as lipid-lowering agent?].

Hypercholesterolemia is one of the major risk factors for ischemic heart disease and for the development of atherosclerotic plaques. Water soluble plant fibers do exert a binding of intestinal cholesterol and are not digested or metabolized. We have investigated the effect of a highly water soluble fiber containing oat brain on serum cholesterol concentrations in 14 volunteers (nine males, five females, age 39 to 67 years, serum cholesterol concentration: 7.14 +/- 0.80 mmol/l; x +/- SD) during an intervention with 50 g oat brain per day for nine weeks. We have documented in the whole study population a modest, but significant reduction of serum cholesterol levels of 4.2% (p less than 0.05) at six weeks; however at nine weeks the efficacy of this regimen was less pronounced (3.2%, p = n.s.) speaking for a decreased compliance although this regimen was well tolerated and accepted. In subsets of high risk volunteers for coronary heart disease of male gender (n = 9), with hypercholesterolemia (n = 8) or essential hypertension (n = 8) the reduction of serum cholesterol levels was more consistent (5.6%, p less than 0.05) with no change in normolipemic volunteers.

Adult↗
PubMed1989

Hypertensive dysregulation and its modification by calcium channel blockade in nonoliguric renal failure.

UNLABELLED: To investigate the pathogenetic constellation and its modification by calcium channel blockade in hypertension associated with chronic nonoliguric renal failure, blood pressure (BP), various pressor factors or correlates, cardiovascular responsiveness, and plasma atrial natriuretic peptide (ANP) were assessed in 15 hypertensive patients (serum creatinine 160-715 mumol/l) before and after 6 weeks of intervention with the agent nitrendipine. On placebo, these patients had a lower plasma angiotensin II (AngII) clearance and higher values of supine plasma AngII, aldosterone, norepinephrine (NE), and heart rate than healthy humans. Acute responses of BP to AngII and of heart rate to isoproterenol were blunted in the patients (p less than 0.05-0.001). Plasma ANP was elevated, correlated positively with systolic BP, and rose in response to NE pressor infusion (p less than 0.05-0.001). Exchangeable sodium and blood volume did not differ significantly from normal values. Nitrendipine reduced the cardiovascular responses to AngII, NE, and isoproterenol and lowered supine BP from 173/102 +/- 5/2 to 146/81 +/- 3/3 mm Hg and upright BP from 170/105 +/- 5/2 to 145/86 +/- 4/3 mm Hg (p less than 0.05-0.001); except for slightly increased plasma AngII, the levels of other endocrine variables, exchangeable sodium, blood volume, and creatinine clearance were not significantly modified. CONCLUSIONS: Hypertension accompanying chronic nonoliguric renal impairment seems to be strongly AngII and probably also NE dependent. Circulating ANP levels are high in this setting. Calcium channel blockade with nitrendipine effectively reduces cardiovascular AngII and NE dependence and BP.

Adult↗
PubMed1988

Human growth hormone in urine: development of an ultrasensitive radiometric assay.

An immunoradiometric assay for human growth hormone (HGH) has been developed which has a detection limit of 1 ng/l and can measure HGH in unextracted urine from normal children and adults. The assay is based on a two-step procedure, using a solid-phase goat-anti-HGH immunosorbent for immunoextraction and [125I]-labeled monoclonal HGH-antibody for detection and quantification. The assay is not affected by urea, NaCl or changes of pH from 5-8. The mean urine HGH concentration in normal children is 6.78 +/- 7.6 (SD) pg/ml, in patients with HGH-deficiency 1.3 +/- 0.9 pg/ml which increases to 11.7 +/- 13.4 pg/ml on the day of growth hormone injection.

Evaluation Studies as Topic↗
PubMed1986

Atrial natriuretic peptide and atrial pressure in patients with congestive heart failure.

To define the relation between atrial pressures and the release of atrial natriuretic peptide, we measured plasma concentrations of the peptide in 26 patients with cardiac disease--11 with normal atrial pressures and 15 with elevated atrial pressures (11 of these 15 had elevated pressures in both atria). Mean peptide levels (+/- SEM) in the peripheral venous blood were increased in the 11 patients with cardiac disease and normal atrial pressures, as compared with 60 healthy controls (48 +/- 14 vs. 17 +/- 2 pmol per liter). In the patients with elevated atrial pressures, peptide concentrations were increased twofold in peripheral venous, right atrial, pulmonary arterial, and systemic arterial plasma, as compared with the concentrations in the patients with normal atrial pressures. A step-up in peptide concentration was seen between the venous and right atrial plasma (P less than 0.002) and between the pulmonary and systemic arterial plasma (P less than 0.01), suggesting release of the peptide from the atria. A linear relation was found between right atrial pressure and right atrial peptide concentration (r = 0.835, P less than 0.001) and between pulmonary wedge pressure and the systemic arterial peptide concentration (r = 0.866, P less than 0.001). Right atrial pressure and the peptide concentration both increased with exercise testing in the nine patients evaluated. We conclude that the release of atrial natriuretic peptide is at least partly regulated by right and left atrial pressures. Distinguishing the relative contributions of the two atria and defining the role of peptide release in the pathogenesis of heart failure will require further investigation.

Adult↗
PubMed1986

Enhanced platelet cyclic AMP response to prostaglandin E1 in essential hypertension.

Platelets provide an accessible and homogeneous cellular system for investigative studies on hypertension. Hypertension-associated abnormalities of cyclic adenosine 3',5'-monophosphate (AMP) metabolism were studied in human platelets. Platelets from hypertensive subjects had an enhanced cyclic AMP accumulation response to prostaglandin E1 (twofold increase in prostaglandin E1 sensitivity). The degree of adenylate cyclase activation in response to both prostaglandin E1 (receptor-mediated) and forskolin (non-receptor-mediated) was greater in hypertensive than normotensive subjects, and prostaglandin E1-stimulated and forskolin-stimulated adenylate cyclase activity correlated directly (r = 0.71, p less than 0.001, n = 26). This finding suggests that the catalytic subunit of the enzyme is the rate-limiting step of this hormonal information transduction. Platelets from hypertensive subjects were more sensitive to epinephrine-induced inhibition of the stimulatory effects of prostaglandin E1 on both cyclic AMP accumulation (fourfold) and activation of cyclic AMP-dependent protein kinase. These findings suggest that the enhanced cyclic AMP metabolic response to prostaglandin E1 in platelets from subjects with established essential hypertension may function as a negative feedback mechanism to protect the cells against calcium overload and to reduce their stimulated participation in hemostatic and thrombotic processes.

Adult↗
PubMed1985

Human cardiac plasma concentrations of atrial natriuretic peptide quantified by radioreceptor assay.

The presence of high affinity receptors for atrial natriuretic peptide in bovine adrenal cortex has enabled the development of a sensitive, specific and rapid radioreceptor assay for this peptide in human plasma. In 18 normal subjects, venous plasma atrial natriuretic peptide concentration ranged from 6 to 65 pM. This plasma concentration was two-fold higher in right atrium as compared to venous blood in 12 patients investigated by cardiac catheterisation, confirming that the right atrium is the site of release of atrial natriuretic peptide into circulation. There was a further step up in plasma atrial natriuretic peptide concentration between pulmonary arterial and aortic plasma. This finding indicates that released hormone in man may undergo further activation in the lungs, or that there may be direct release from the left atrium.

Adrenal Cortex↗
PubMed1985

Platelets and hypertension.

Various physiological changes of platelets and the vascular smooth muscle cell are intimately related. For this reason, in addition to the number of features in common between platelets and vascular smooth muscle and the increased risk for thromboembolic complication in essential hypertension, the platelet was used as an experimental model for the investigation of calcium-dependent functional anomalies associated with hypertension. It is demonstrated, by a sequential analysis of receptor and postreceptor events, that platelets in hypertension exhibit (a) a greater adenylate cyclase-activation and c-AMP-accumulation response to PGE1, (b) an enhanced epinephrine-induced phosphorylation response, and (c) an increased shape change sensitivity to serotonin and epinephrine. The anomalies in these calcium-dependent processes are linked to elevated free calcium concentrations in platelets from hypertensive subjects.

Adenylyl Cyclases↗
PubMed1985

Inhibition of [3H]Gpp(NH)p release from human platelet membranes by GDP.

Previous reports have described hormone-stimulated release of radiolabeled guanine nucleotides from prelabeled membranes. In this paper, we report the inhibition by GDP of both hormone-independent and hormone-specific stimulation of [3H]Gpp(NH)p release from human platelet membranes. This inhibition was shown to be concentration specific and suggests a more complex mechanism of [3H]Gpp(NH)p release than was previously thought. A model is proposed in which guanosin triphosphates cause dissociation of the subunits of the guanine nucleotide binding protein, whereas guanosine diphosphate prevents this dissociation resulting respectively in stimulation or inhibition of the release of bound [3H]Gpp(NH)p.

Blood Platelets↗
PubMed1985

Activation of human blood platelets by arginine-vasopressin. Role of bivalent cations.

Arginine-vasopressin caused platelet activation, i.e., a shape change reaction and a rise in intracellular free Ca2+ ([Ca2+]i) only in the presence of certain bivalent cations. The EC50 of arginine-vasopressin (concentration causing half-maximal shape change) decreased with rising concentrations of Mn2+, Mg2+, or Ca2+ in the medium, but was at least an order higher with Ca2+ than with Mn2+ or Mg2+. The EC50 of the active bivalent cations (concentrations enabling 100 nM arginine-vasopressin to exert half-maximal shape change and rise in [Ca2+]i) varied with the individual cations, being by far the highest for Ca2+. The KD of [3H]arginine-vasopressin binding to platelet membranes and intact platelets markedly decreased when extracellular Mg2+ or Mn2+ were present, and the KD values were inversely related to the concentration of the cations. Ca2+ also lowered the KD values; however, the effect was less marked than that of Mg2+ or Mn2+ and, in physiological conditions, significant only in intact platelets. Vasopressin-1 antagonists counteracted arginine-vasopressin binding and the shape change reaction and [Ca2+]i rise induced by arginine-vasopressin. In the presence of Mn2+ in the medium, administration of arginine-vasopressin led to quenching of the intracellular fluorescence of 2-methyl-6-methoxy-8-nitroquinoline-loaded platelets, possibly due to influx of Mn2+. In conclusion, the dependency of the arginine-vasopressin-induced platelet activation on bivalent cations is at least partly due to an enhancement by these cations of the affinity of the vasopressin-1 receptor for arginine-vasopressin. Thereby, under physiological conditions, Mg2+ seems to be of primary importance. Other mechanisms may be involved, too, e.g., an enhancement by arginine-vasopressin of the influx of bivalent cations into the platelets.

Aminoquinolines↗
PubMed1984

Correlation of platelet calcium with blood pressure. Effect of antihypertensive therapy.

Intracellular free calcium has been implicated in vascular smooth-muscle contraction and in the pathophysiology of essential hypertension. We studied free-calcium levels in blood platelets, which have many features in common with vascular smooth-muscle cells. With use of an intracellularly trapped fluorescent dye, the free-calcium concentration in platelets was found to be elevated in 9 patients with borderline hypertension and 45 patients with established essential hypertension, who were compared with 38 normotensive subjects. There was a close correlation between the free-calcium level and both systolic and diastolic blood pressure (n = 92; r = 0.883 for systolic pressure and 0.931 for diastolic pressure; P less than 0.001 for both). Antihypertensive treatment with calcium-entry blockers (n = 15), beta-adrenoceptor blockers (n = 12), or a diuretic (n = 6) resulted in a reduction in free calcium, and this correlated with the fall in blood pressure (P less than 0.001). The intracellular free-calcium concentration in platelets may be determined by the same humoral or pharmacologic factors that determine the height of blood pressure.

Adolescent↗
PubMed1984

Inappropriate correction for radioactive decay in fully iodinated adrenergic radioligands.

The present data demonstrate increased binding of various iodinated adrenergic radioligands. In contrast, this was not observed for [3H]dihydroalprenolol. This systematic deviation of apparent binding parameters can be explained by the inappropriate use of a decay correction factor, indicating that the decayed iodinated radioligands lose their binding ability. Consequently no correction for decay is required in the case of iodinated adrenergic radioligands.

Animals↗
PubMed1984

Enhancement of calcium influx in human platelets by CGP 28392, a novel dihydropyridine.

CGP 28392, a novel compound structurally related to the dihydropyridine Ca2+-entry blockers, causes a dose-dependent increase in intracellular free Ca2+ in human platelets, as measured with the Quin-2 Ca2+ indicator, with a semimaximal effective concentration of 2.2 X 10(-7) M. This effect occurs in a concentration range in which CGP 28392 competes for specific [3H]nitrendipine binding in guinea pig heart membranes. It can be inhibited by nitrendipine. The data presented furnish direct evidence of the Ca2+-entry-stimulating properties of CGP 28392 and indicate the presence of dihydropyridine-susceptible structures in human platelets.

Animals↗
PubMed1984

Ca2+ as messenger of 5HT2-receptor stimulation in human blood platelets.

In blood platelets of man, both 5-hydroxytryptamine (5HT) and 80 nM of the Ca2+-ionophore A23187 led to rapid shape change reactions which were inhibited by prostaglandin E1 (PGE1), forskolin, 2-methyl-6-methoxy-8-nitroquinoline ( quin2 ) and chlortetracycline. The IC50-values of the inhibitors were similar in the 5HT- and the A23187-experiments. Higher amounts of A23187 abolished the inhibitory actions of PGE1 and forskolin. Furthermore, 5HT and A23187 enhanced adrenaline-induced platelet aggregation their effects showing similar time dependence. Ketanserin, an antagonist of 5HT2 -receptors, and 8-(N,N-diethyl-amino)octyl-3,4,5-trimethoxybenzoate (TMB-8), an intracellular Ca2+-antagonist, counteracted the effects of 5HT much more than those of A23187, whereas acetylsalicylate and indomethacin did not influence the actions of either 5HT or A23187. In addition, 5HT caused a concentration-dependent rise of intracellular free Ca2+ in platelets which was counteracted by ketanserin. PGE1 and forskolin reduced the resting Ca2+-levels. 5HT did not affect either the basal or the PGE1-stimulated activity of adenylate cyclase, whereas the Ca2+-ionophore A23187 slightly raised the basal activity of the enzyme. In conclusion, the functional effects of 5HT2 -receptor stimulation in human blood platelets (shape change reaction and enhancement of adrenaline aggregation) seem to be mediated by a rise of intracellular free Ca2+.

Adenylyl Cyclases↗
PubMed1984

Beta-adrenergic receptors are different in subpopulations of human circulating lymphocytes.

Mononuclear leucocytes (MNL) were isolated from blood of 11 healthy blood donors. Lymphocyte subsets were sorted in a Cytofluorograf after direct (B cells) or indirect immunofluorescence labeling with monoclonal antibodies directed against the phenotypes of T-, T helper (Th)- and T suppressor (Ts) cells. The sorted cells were incubated with (+/-)125iodocyanopindolol ([125I]CYP) for the determination of beta-adrenergic receptors. Beta-adrenergic receptors on B cells were increased two-fold (3700 sites/cell, p less than 0.004) and had a lower affinity (dissociation constant KD 40pM, p less than 0.03) when compared with T cells (1400 sites/cell, KD 17pM). Receptors on Th- and Ts cells showed a similar binding capacity, but Ts cells had a slightly higher [125I]CYP binding affinity (KD 13 pM) than Th cells (KD 27 pM, p less than 0.02). The different densities and affinities of beta-adrenergic receptors in human lymphocyte subsets, as assessed by antagonist binding should be considered in the interpretation of receptor alterations of unfractionated MNL, which may occur simultaneously to changes of the blood leucocyte distribution.

Adult↗
PubMed1984

Methods for the determination of the specific radioactivity of radioligands.

Quantitative analysis of radioligand binding data requires the knowledge of an accurate and actual value for the specific radioactivity of the radiolabeled ligand. Several protocols, based on simple radioligand binding experiments, which allow the determination of the molar assay concentration of the radioligand and of the radioligand/receptor complex, are described. Their appropriateness is demonstrated by the use of tritiated and iodinated beta-adrenergic radioligands.

Animals↗
PubMed1984

Measurement of receptor induced changes in intracellular free calcium in human platelets.

The intracellular free calcium concentration plays a key role as second messenger in the regulation of cellular reactions. Post-receptor events can be investigated by measurement of free calcium concentration in cells. Our experience in measuring the intracellular free calcium concentration in platelets with the use of the fluorescent indicator quin-2-tetraacetoxymethyl- ester is described. Possible pitfalls in the preparation procedures of the platelets are discussed as well as critical steps and the limitations of the quin-2-method. The methodological approach is demonstrated by the presentation of an investigation with the adenylate cyclase inhibitors adenosine-5'-diphosphate and epinephrine as well as their interrelationship. The potentiation effect of epinephrine to adenosine 5'-diphosphate on platelet function such as aggregation is accompanied by a potentiation of the effect of these two platelet activators in elevating the intracellular free calcium concentration. Adenosine 5'-diphosphate elevates intra-platelet free calcium alone, whereas epinephrine acting through stimulation of the alpha2-receptor needs another permissive factor to immediately elevate the intra-platelet free calcium.

Adenosine Diphosphate↗